Glomerular diseases mostly presenting with Nephritic syndrome
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1 Glomerular diseases mostly presenting with Nephritic syndrome 1
2 The Nephritic Syndrome Pathogenesis: proliferation of the cells in glomeruli & leukocytic infiltrate Injured capillary walls escape of RBCs into urine GFR oliguria, fluid retention, and azotemia. Hypertension (a result of both the fluid retention and some augmented renin release from kidneys). 2
3 1- Membranoproliferative Glomerulonephritis (MPGN ) Abnormal proliferation of glomerular cells. Usually nephritic syndrome; others have a combined nephrotic-nephritic picture. Types of MPGN: 1-type I (80% of cases) immune complex disease (The inciting antigen is not known) 2-type II excessive complement activation 3
4 Type I MPGN circulating immune complexes Many associations :hepatitis B and C; SLE; infected A-V shunts. 4
5 Type II MPGN (dense-deposit disease) Cause: excessive complement activation autoantibody against C3 convertase called C3 nephritic factor (it stabilizes the enzyme and lead to uncontrolled cleavage of C3 and activation of the alternative complement pathway). Result: Hypocomplementemia 5
6 Morphology LM both types of MPGN are similar by LM. glomeruli are large with accentuated lobular appearance and show proliferation of mesangial and endothelial cells as well as infiltrating leukocytes GBM is thickened (double contour or "tram track" ) The tram track appearance is caused by "splitting" of the GBM 6
7 silver stain -double contour of the basement membranes("tramtrack" ) that is characteristic of (MPGN)(arrows). 7
8 IF Type I MPGN subendothelial electrondense deposits (IgG and early complement components (C1q and C4) Type II MPGN C3 is deposited in an irregular pattern. 8
9 EM- dense deposits in the basement membrane of MPGN type II in a ribbon-like mass (arrows) 9
10 Clinical Course prognosis poor. No remission. 40% progress to end-stage renal failure. 30% had variable degrees of renal insufficiency. Dense-deposit disease (type II) has a worse prognosis. It tends to recur in renal transplant recipients 10
11 2- Acute Postinfectious (Poststreptococcal) Glomerulonephritis (PSGN) deposition of immune complexes + proliferation of glomerular cells and leukocytes ( neutrophils). Not direct infection of the kidney Causes: poststreptococcal GN (most common). Infections by other organisms as pneumococci and staphylococci 11
12 Poststreptococcal GN It develops 1-4 wks after the individual recovers from a group A streptococcal infection. Only certain "nephrito-genic" strains of β- hemolytic streptococci are capable of glomerular disease. In most cases pharynx or skin infection. Mechanism: binding of immune complexes or antibodies to bacterial antigens planted in the GBM. 12
13 LM uniformly increased cellularity of the glomerular tufts (proliferation of endothelial and mesangial cells and neutrophilic infiltrate). IF deposits of IgG and complement within the capillary walls and mesangial areas. EM immune complexes subepithelial "humps" in GBM. 13
14 Post-streptococcal glomerulonephritis is due to increased numbers of epithelial, endothelial, and mesangial cells as well as neutrophils in and around the capillary loops (arrows) 14
15 Clinical Course acute onset. fever, nausea, and nephritic syndrome. gross hematuria. Mild proteinuria. Serum complement levels are low during the active phase of the disease. serum anti-streptolysin O antibody titers. Recovery occurs in most children. 15
16 3- IgA Nephropathy (Berger Disease) one of the most common causes of recurrent microscopic or gross hematuria children and young adults. episode of hematuria 1 or 2 days after nonspecific upper respiratory tract infection. hematuria lasts several days and then subsides and recur every few months. 16
17 Pathogenesis abnormality in IgA production and clearance. LM: variable focal proliferative GN; diffuse mesangial proliferation or crescentic GN. IF mesangial deposition of IgA with C3 EM deposits in the mesangium 17
18 IF :IgA mesangial staining. 18
19 Rapidly Progressive (Crescentic) Glomerulonephritis 19
20 Rapidly Progressive (Crescentic) Glomerulonephritis characterized by the presence of crescents (crescentic GN). proliferation of the parietal epithelial cells of Bowman's capsule in response to injury and infiltration of monocytes and macrophages nephritic syndrome rapidly progresses to oliguria and azotemia. 20
21 Pathogenesis Type I (Anti-GBM Antibody): (12%) linear deposits of IgG and, C3 on the GBM. Anti-GBM antibodies are present in the serum and are helpful in diagnosis. Plasmapheresis which removes pathogenic antibodies from the circulation is beneficial 21
22 Type II (Immune Complex) (44%): Idiopathic E.g. SLE, Henoch-Schönlein purpura/iga nephropathy, etc Type III (Pauci-Immune) ANCA Associated (44% ): Idiopathic E.g. Wegener granulomatosis; Microscopic angiitis
23 Crescentic GN (PAS stain). the collapsed glomerular tufts and the crescent-shaped mass of proliferating cells and leukocytes internal to Bowman's capsule. 23
24 IF According to type: Type 1 linear IgG along GBM Type 2 Igs and complements Type 3 no deposits EM According to type: Type 1 no deposits Type 2 immune complexes Type 3 no deposits 24
25 Chronic Glomerulonephritis Among all chronic renal failure, 30% to 50% result from chronic GN. the end stage of any glomerular disease Morphology = end-stage kidneys kidneys are symmetrically contracted. LM scarring of glomeruli, interstitial fibrosis; tubular atrophy; thick-walled, narrowed blood vessels 25
26 Chronic GN. A MT stain shows complete replacement of virtually all glomeruli by blue-staining collagen. 26
27 27 Hereditary Nephritis
28 a group of hereditary glomerular diseases caused by mutations in GBM proteins (most common X-linked). Most important type: Alport syndrome: Alport syndrome = nephritis + nerve deafness + eye disorders, including lens dislocation, posterior cataracts, and corneal dystrophy. Pathogenesis: Mutation of any one of the α chains of type IV collagen overt renal failure occurs between yrs of age 28
29 EM GBM thin and attenuated GBM later develops splitting and lamination "basket-weave" appearance 29
30 Basket weave GBM in Alport syndrome 30
31 Disease Presentatio n Age LM IF EM Prognosis MCD nephrotic Children none negative Effaced foot processes FSGS nephrotic adults Segmental sclerosis negative Effaced foot processes MNP nephrotic adults Thickened GBM IgG+C3+ Sub-epithelial spikes and domes good Poor? Poor? MPGN-type1 nephritic adults Tram track Igs Subendothelial deposits poor MPGN-type2 nephritic adults Tram track C3+ Dense deposits poor IgA nephropth nephritic Children, young adults variable IgA+ Mesangial deposits variable PSGN nephritic children hypercellularity IgG+ C3+ Subepithelial deposits (humps) good Alport syndrome hematuria, hearing loss children variable negative Basket weave GBM poor 31
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